Re:lactation ketoacidosis-bmj case report

Arthur J Henderson, Retired Researcher

none

Ketoacidosis is a direct result of exteremly low cellular magnesium
levels. Gluconeogenesis is impaired at Glucose6 Phosphatase G6-Pase. G6-
Pase is very magnesium dependent so if magnesium levels are severely
reduced blood glucose levels plummet starving neurons of energy. The
neurons in the hypothalamus signal the gut get more in 'the hunger pangs
in Obesity'.
Pyruvate carboxylase is also very magnesium dependent and if impaired by
low magnesium levels and will also shutdown gluconeogenesis. Ketoacidosis
is a direct result of beta oxidation of fat converting to AcetylCoA and
Ketones. This continuous manufacture of ketones results in acid blood.
Kidney failure in severe obesity and Diabetes-2 are other complications
caused by a failure of gluconeogenesis.
A magnesium sulphate injection would rectify the condition in amatter of
minutes. If you require a comprehensive article please email. Arthur
Henderson

Conflict of Interest:

Re:lactation ketoacidosis-bmj case report

Adam Szulewski

Queen's University Department of Emergency Medicine Kingston General Hospital

Thank you for your interest in our paper and for your comments. As
was correctly pointed out in the letter, patients who are kept NPO should
be given IV glucose supplementation. This was not done for our patient and
this is indeed one of the reasons we decided to present her case in the
Learning from errors section of the journal.
We would like to clarify that it is in fact very unlikely for a non-
breastfeeding patient to become significantly acidotic secondary to having
no caloric intake for three days. Our bodies are normally well equipped to
deal with short term starvation and only mild levels of acidosis develop
in the starvation state when insulin levels are normal. In a small study
published by Reidenberg et al., obese (non-lactating) women were starved
for over a month and this produced only a mild metabolic acidosis of
approximately 7.35 on arterial blood gas analysis. 1 On the other hand,
Mohammad et al. showed that when lactating women are fasting for more than
42 hours, they begin to rely almost exclusively on gluconeogenesis as an
energy substrate for milk production and are therefore at greater risk to
develop a more profound metabolic acidosis compared to non-lactating
women. 2 This distinction is key in our patient's case and emphasizes the
unique nutritional needs of breastfeeding women.
We hope this clarifies the issue.
Adam Szulewski
1. Reidenberg MM, Haag BL, Channick BJ, et al. The Response of Bone to
Metabolic Acidosis in Man. Metabolism 1966;15:236-241.
2. Mohammad MA, Sunehag AL, Chacko SK, et al. Mechanisms to conserve
glucose in lactating women during a 42-h fast. Am J Physiol Endocrinol
Metab 2009;297:E879-88.

Conflict of Interest:

lactation ketoacidosis-bmj case report

mahesh masand, consultant paediatrician

Dr Grays hospital,Elgin

It was indeed a very interesting report to read and was actually
fascinated with the title initially. After reading the case report I am
tempted to make some comments on the title which may be quite misleading
.Even a normal person( meaning who is not breast feeding) will become
ketotic if made nil by mouth for whatever reason for 3 days .But here the
breast feeding probably aggravated the process further so it is difficult
to say that the patient became ketotic because of breast feeding . I have
been informed by the author that it is not their normal policy to keep a
patient NPO for 3 days and not give any glucose so I am still not clear
as to the reason for not giving IV glucose to this lady who wanted to
continue breast feeding while she was NPO as that would not have been
contraindicated .Yes I would agree with the author that this is a case of
iatrogenic starvation acidosis but that would have developed in any person
whether breast feeding or not after being kept NPO for 3 days .